Hypercapsule is the cornerstone of in inducing pyogenic liver abscess.

PURPOSE

To investigate the mechanisms of -induced pyogenic liver abscess (PLA).

METHODS

Forty-three strains from PLAs and 436 from non-PLAs were collected. Their differences were compared for virulence genes and factors, sequence types, and serotypes. Virulence genes , , and + were deleted in NTUH-K2044. Various analyses, such as transmission electron microscopy, neutrophil killing tests, and mouse lethality tests, were used to confirm the consequent changes.

RESULTS

Differences were found between strains from PLA and non-PLA samples for virulence genes and factors, including metabolism genes ( and ), capsular polysaccharide (CPS)-synthesis channel gene (), CPS-regulating genes (, , and ), and siderophore genes ( and ). When was positive, the difference between PLA and non-PLA samples was only observed with . Δ, Δ, and ΔΔ strains reverted to hypovirulence. In the Kupffer cell stimulation assay, interleukin (IL)-6, IL-12, IL-10, and transforming growth factor-β secretions were found to be equivalent in NTUH-K2044, Δ, Δ, and ΔΔ groups. Lower IL-1β and higher tumor necrosis factor-α secretions were observed for Δ, Δ, and ΔΔ.

CONCLUSIONS

Hypercapsule production is the cornerstone of hypervirulence, regardless of exopolysaccharides. K1 -induced PLA may decrease core inflammatory cytokines rather than increase anti-inflammatory cytokines. Exopolysaccharides could also attenuate the inflammatory response to aid in the immune escape of .